Author(s): Kornél Simon
The stress reaction (acute, repetitive or chronic stress patterns) is a non-specific response of an organism to a pathological state. The metabolic characteristics of these stress patterns are well documented. Recognizing the interrelation between a stress-induced pathological state and the relevant pattern of the resultant stress reaction can provide a more accurate assessment of actual cellular metabolism than an approach relying on blood glucose values. Stress activation is obligatorily associated with negative energetic balance in affected cellular metabolism, which is reversed by elimination of the stressor. Prolongation of the stress reaction is a marker indicating the ineffective elimination of the causal stressor. Chronic stress induces progressive self-generating cellular metabolic dysfunction, resulting in the development of both diabetic and ischaemic disorders. Chronic stress conditions are characterized by reductions in inducible metabolic capacity, acute stress tolerance, and functional performance, accompanied by stress-specific micro- and macroscopic alterations. Chronic stress can be activated by both somatic and psychomental stressors. Diabetes, starvation, obesity, ageing, pregnancy, and any chronic disease state of a vital organ are associated with activation of stress reaction. The increased susceptibility of diabetic patients on gliflozins to the development of postoperative euglycaemic ketoacidosis can be explained by a reduction in chronic stress-associated acute stress tolerance, related mainly to diabetes, and a relative glucose deficiency induced by gliflozin therapy. Chronic hyperglycaemia associated with chronic stress should be considered both the primary cause and the secondary consequence of cellular dysmetabolism. Achievement of near-normoglycaemia is a beneficial effect but is not a causal intervention
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